Aspirin-exacerbated respiratory disease (AERD) refers to the development of bronchoconstriction in asthmatics following the exposure to aspirin or other nonsteroidal anti-inflammatory drugs. The key pathogenic mechanisms associated with AERD are the overproduction of cysteinyl leukotrienes (CysLTs) and increased CysLTR1 expression in the airway mucosa and decreased lipoxin and PGE2 synthesis. Genetic studies have suggested a role for variability of genes in disease susceptibility and the response to medication. Potential genetic biomarkers contributing to the AERD phenotype include HLA-DPB1, LTC4S, ALOX5, CYSLT, PGE2, TBXA2R, TBX21, MS4A2, IL10, ACE, IL13, KIF3A, SLC22A2, CEP68, PTGER, and CRTH2 and a four-locus SNP set composed of B2ADR, CCR3, CysLTR1 , and FCER1B . Future areas of investigation need to focus on comprehensive approaches to identifying biomarkers for early diagnosis.
Shrestha Palikhe, N., Kim, S.-H., Jin, H. J., Hwang, E.-K., Nam, Y. H., & Park, H.-S. (2011). Genetic Mechanisms in Aspirin-Exacerbated Respiratory Disease. Journal of Allergy, 2012, 1–6. https://doi.org/10.1155/2012/794890